An Atlas of Gross Pathology - C. Fletcher, P. McKee (Edward Arnold, 1987) WW

113 Pages·1987·63.73 MB·English

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British Library Cataloguing in Publication Data:

Fletcher, Christopher D.M.
An atlas of gross pathology.
1. Pathology
I. Title II. McKee, Phillip H.
616.07 RBll1

ISBN: 0-906923-47-6 (Gower)
0-7131-4557-9 (Arnold)

©Copyright 1987 by Gower Medical Publishing Limited.
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illustration: Pamela Corfield

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Preface

The aim of this atlas is to provide an introduction to
the macroscopical appearances of the most common
pathological conditions for undergraduate medical
students and nurses in training. It will also, hopefully,
be of value to postgraduates undertaking the FRCS
examinations, for whom a working knowledge of
gross pathology is vital .

Only important or frequently encountered disease
processes are covered. Each illustration is
accompanied by a concise legend outlining basic,
relevant clinicopathological and pathogenetic
details. In collecting material for this atlas, we are
deeply indebted to Professor J.R. Tighe of the
Histopathology Department at St. Thomas's Hospital
for allowing us access to the departmental collection
of colour transparencies. Weare also particularly
grateful to Dr H. Pambakian, Museum Curator at St.
Thomas's Hospital Medical School and Professors H.
Spencer and M.S.R. Hutt. Most of all, this book would
not have been possible without the consistent
generosity and thoughtfulness of all the pathologists
in our department, who unselfishly offered us many
of their specimens, obtained either surgically or at
post mortem, for photography.
.

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COM Fletcher & PH McKee
London

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111 .

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Acknowledgements

,

The authors would like to thank the following
colleagues for providing illustrative material:
Professor P.G. Bullough, Cornell University Medical
College, New York (Figs.7.16 , 12.1 bottom, 12.4,
12.7-12.10,12.13-12.15,12.17,12.18, 12.20-22,
12.24, 12.25 & 12.29 top); Dr D.W. Day, Dept. of
Pathology, University of Liverpool Medical School,
Liverpool (Fig.3.23 ); DrC.W. Elston, Dept. of
Pathology, City Hospital, Nottingham (Fig.9.35);
Profossor P.L. lantos, Dept. of Neuropathology,
Institute of Psychiatry, London (Figs. 11. 1 0, 11.20 &
11.24); Dr].C. Macartney, Dept. of Histopathology,
St Thomas's Hospital Medical School, London
(Figs.4.26, 4.29, 7.8 & 12.26); Professor F.V. O'Brien,
School of Dentistry, Queen's University, Belfast
(Figs.3.1 & 3.2); Dr C. Parkinson,"Institute of
Urology, London (Figs. 10.7 & 10.13); DrD.E.
Sharvill, William Harvey Hospital, Ashford, Kent
(Fig. 5.13 ); Dr ].M. Sloan, Senior Lecturer/Consultant
Pathologist, Royal Victoria Hospital, Belfast (Figs.2.3,
2.4,2.14,8.24 & 8.30); The Wellcome Museum,
Royal College of Surgeons of England, London
(Figs.8.20 & 9.28).

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III Ii 1IIIIwing

Contents

Preface
Acknowledgements

1 Cardiovascular System
2 Respiratory System

3 Alimentary System
4 HepatobiliarySystem
5 Breast

6 Lymphoreticular System
7 Endocrine System
8 Urinary System

9 Female Reproductive System
10 Male Reproductive System

11 Nervous System

12 Osteoarticular System
Index

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iv

1

13

23

36

45

50

55

62

72

83

87

94

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103

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1 Cardiovascular System

Fig.1.1 Recent myocardial infarct. A transverse section through
both right and left ventricles, viewed from below. The anterior wall of
the left ventricle shows an extensive area of recent infarction, charac­
terised by an almost full-thickness zone of yellow necrotic myo­
cardium, surrounded by a hyperaemic rim . The latter consists of
granulation tissue (capillaries and fibroblasts) and represents the
early phase of healing. This infarct is of approximately one week's
duration. In nearly all cases, myocardial infarction is caused by
occlusive thrombosis in an atheromatous coronary artery. Rare
causes include syphilitic aortitis, polyarteritis nodosa and coronary
artery embolism from a variety of cardiac lesions.

Fig.1.2 Healed myocardial infarct. The heart has been opened to
display the inner aspect of the left ventricle. Marked pale fibrous
scarring is seen in the posterior wall and in the papillary muscles.
Mural thrombus overlying the scar is also present. Healing, by
fibrosis, commences about 3 weeks after acute infarction and is
usually complete after 2 months. Fibrous replacement of the myo­
cardium predisposes to aneurysm formation (see Fig .1.6) within
'vhich thrombus may form.

Fig.1.3 Coronary artery thrombosis. The left main stem coronary
artery has been opened longitudinally to reveal occlusion of its lumen
by thrombus (arrowed). Note the presence of atheroma in the
ascending aorta and a fibrinous pericarditis. Occlusive coronary
thrombosis almost always occurs at the site of an atheromatous
stenosis (see Figs.1.36-1 .38) and is thought to be initiated either by
ulceration or haemorrhage into a plaque.

Fig.l.4 Coronary
artery thrombosis.
The left anterior
descending coron­
ary artery is shown in
transverse section.
The lumen is mark­
edly diminished by
atheroma, and over­
lying thrombus has
resulted in total occ­
lusion. In the vast
majority of cases of
myocardial infarc­
tion, such occlusive
thrombosis will be
detected if the
coronary arteries are
examined with suffi­
cient care.

Fig.1.5 Myocardial infarct with mural thrombulI '''''' ~
rupture. The heart has been opened to expo:'!!) III" 'jill ,II
left ventricle. A large mural thrombus is adhOlull1 Il ' lLI l !Il
myocardial infarction, complicated by rupture (111I1I ! illli ll
septum. The probe has been passed through II" , It 11110 II '
extreme left of the pictu re its tip can be seen IIV' !lIYII II I II "
ventricular flap. Myocardial rupture, which is not III II "II it '
occurs within a week of acute infarction,

Flg.l.S Left ventricular aneurysm. The d(~ vO IIlI'"1I 11 11 ,
aneurysm of the left ventricle is a not uncomllliJlt 111 111 1 III '
myocardial infarction. It is due to replacemellt (11111 ) I"Y"
collagenous scar tissue with resultant loss of 0111;,111 ily 'II
aneurysms often contain mural thrombus whic:h " Illy I II
systemic emboli. The laceration of the anterior' IlilllllllllY "
right of the aneurysm occurred during the post 1111111,,,,,

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1 Cardiovascular System

left main stem coronary
occlusion of its lumen
of atheroma in the
. Occlusive coronary
of an atheromatous
to be initiated either by

Fig.1.4 Coronary
artery thrombosis.
The left anterior
descending coron­
ary artery is shown in
transverse section.
The lumen is mark­
edly diminished by
atheroma, and over­
lying thrombus has
resulted in total occ­
lusion. In the vast
majority of cases of
myocardial infarc­
tion, such occlusive
thrombosis will be
detected if the
coronary arteries are
examined with suffi­
cient care.

Fig.1.5 Myocardial infarct with mural thrombus and ventricular
rupture. The heart has been opened to expose the septal wall of the
left ventricle. A large mural thrombus is adherent to an area of recent
myocardial infarction, complicated by rupture of the interventricular
septum. The probe has been passed through the rupture and at the
extreme left of Ihe picture its tip can be seen overlying the righl
ventricular flap. Myocardial rupture, which is not uncommon, usually
occurs within a week of acute infarction .

Fig.1.6 Left ventricular aneurysm. The development of an
aneurysm of the left ventricle is a not uncommon late complication of
myocardial infarction. It is due to replacement of the myocardium by
collagenous scar tissue with resultant loss of elasticity. Such
aneurysms often contain mural thrombus which may be a source of
systemic emboli. The laceration of the anterior papillary muscle to the
right of the aneurysm occurred during the post mortem.

Fig.1.7 Haemopericardium. The pericardial sac has been opened
(left) to show an extensive haematoma overlying the epicardium. On
the right, the haematoma has been removed to reveal the cause as
being a slil-like ventricular perforation (arrowed) at the site of a recent
myocardial infarct. Haemopericardium may more rarely occur as a
complication of dissecting aortic aneurysm or trauma.

Fig.1.8 Ruptured papillary muscle. The heart has been opened to
display the posterior aspect of the left ventricle. In the centre of the
picture is a portion of the anterior papillary muscle which has been ,
torn and shows obvious necrosis. Rupture of a papillary muscle is a
rare complication of myocardial infarction, which usually occurs
within 2 weeks of the primary event: it results in the acute onset of
mitral incompetence and left ventricular failure.

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1 Cardiovascular System

Fig.1.9 Left ventricular hypertrophy. Left ventricutar hypertrophy
is a not uncommon finding at post mortem owing to the frequency of
essential hypertenSion in the population. A list of causes is given in
Fig:1.10 In this instance the increased thickness of the left ventricular
wall is obvIous (in excess of 20mm) However, a much more accurate
method of assessing venlricular hypertrophy involves weighing the
chambers separately after careful dissection, thereby taking into
account any degree of associated ventricular dilatation.

CAUSES OF LEFT VENTRICULAR HYPERTROPHY

Systemic hypertension

Aortic stenosis

Aortic incompetence

Mitral incompetence

Congenital heart disease
coarctation of aorta

reversed VSD

Amyloid

Cardiomyopathy

anaemia

High output failure
thyrotoxicosis

Paget's disease

A-V malformation
-­
-­
-­
-
-
-­
-­
-­

Fig.1.10 Causes of left ventricular hypertrophy.

Fig.1.11 Acute rheumatic endocarditis. Characteristic small pink
vegetations (arrowed) are present along the line of closure of this
mitral valve cusp. Rheumatic fever, a multisystem autoimmune
process, is a rare complication of (3-haemolytic (Group A) strepto­
coccal infections. It results from the development of heterophilic
cross·reacting antibodies to the streptococcal M protein and an, as
yet unidentified, connective tissue antigen . Manifestations include a
pancarditis, joint involvement, skin rashes, subcutaneous nodules
and , rarely, Sydenham's chorea .

Fig.1.12 Mitral stenosis with atrial thrombus. The commonest
complication of rheumatic endocarditis is mitral stenosis and, indeed,
almost all stenotic mitral valves are of rheumatic origin. Fusion of the
valve cusps and fibrosis results in narrowing of the valve orifice. The
stenosis causes leli atrial dilatation and may be complicated by atrial
fibrillation with consequent thrombus formation, as seen in this case.

Fig.1.13 Mixed mitral valve disease. Therl; 1: , II,.lfl" ,II,
the chordae tendinae wilh fusion and shorte"" ,i I 11" , III'
process has produced a rigid 'buttonhole' valv,' II" ,jO .j 'I
stenotic and incompetent - the latter has resulu)d '" II I'" II
of left ventricular hypertrophy. as seen in th e Ix ,II", II ' If I1 I1
corner.

CAUSES OF MITRAL INCOMPETENCr

Rheumatic heart disease

Papillary muscle rupture or fibrosis

Congenital

Mitral valve prolapse (floppy valvo !,Y'ldJl '" I,

Functional dilatation of valve ring

Marfan's syndrome

.Fig.1.14 Causes of mitral incompetence.

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1 CardiovascularSystem

Fig.1.13 Mixed mitral valve disease. There IS marked fibrosIS 01
the chordae tendinae with fusion and shortening. The rheumatic
process has produced a rigid 'buttonhole' valve, thereby being both
stenotic and incompetent· the latter has resulted in the deve lopment
of lelt ventricular hypertrophy, as seen in the bottom right hand
corner.
I
I
CAUSES OF MITRAL INCOMPETENCE

Rheumatic heart disease

Papillary muscle rupture or fibrosis

Congenital

Mitral valve prolapse (floppy valve syndrome)

Functional dilatation of valve ring

Marfan's syndrome

Fig.1.15 Aortic stenosis. Isolated aortic stenosis may complicate
rheumatic heart disease but more often is associated with mltrat
involvement also. The proximal portion of the ascending aorta has
been opened to view this stenotic valve from above. Aortic stenosis
usually gives rise to left ventricular hypertrophy and may compromise
the coronary blood supply.

Fig.1.16 Calcific aortic stenosis. Calcification of the aortic valve
most commonly occurs in a congenital bicuspid valve, but may also
arise as a consequence of rheumatic disease and is sometimes a
feature of the ageing process. Note the coarse calcific nodules in the
valve cusps
Fig.1.14 Causes of mitral incompetence.

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